
‘I keep away from people’ – combined vision and hearing loss is isolating more and more older Australians
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Our ageing population brings a growing crisis: people over 65 are at greater risk of dual sensory impairment (also known as “deafblindness” or combined vision and hearing loss).
Some 66% of people over 60 have hearing loss and 33% of older Australians have low vision. Estimates suggest more than a quarter of Australians over 80 are living with dual sensory impairment.
Combined vision and hearing loss describes any degree of sight and hearing loss, so neither sense can compensate for the other. Dual sensory impairment can occur at any point in life but is increasingly common as people get older.
The experience can make older people feel isolated and unable to participate in important conversations, including about their health.
Causes and conditions
Conditions related to hearing and vision impairment often increase as we age – but many of these changes are subtle.
Hearing loss can start as early as our 50s and often accompany other age-related visual changes, such as age-related macular degeneration.
Other age-related conditions are frequently prioritised by patients, doctors or carers, such as diabetes or heart disease. Vision and hearing changes can be easy to overlook or accept as a normal aspect of ageing. As an older person we interviewed for our research told us
I don’t see too good or hear too well. It’s just part of old age.
An invisible disability
Dual sensory impairment has a significant and negative impact in all aspects of a person’s life. It reduces access to information, mobility and orientation, impacts social activities and communication, making it difficult for older adults to manage.
It is underdiagnosed, underrecognised and sometimes misattributed (for example, to cognitive impairment or decline). However, there is also growing evidence of links between dementia and dual sensory loss. If left untreated or without appropriate support, dual sensory impairment diminishes the capacity of older people to live independently, feel happy and be safe.
A dearth of specific resources to educate and support older Australians with their dual sensory impairment means when older people do raise the issue, their GP or health professional may not understand its significance or where to refer them. One older person told us:
There’s another thing too about the GP, the sort of mentality ‘well what do you expect? You’re 95.’ Hearing and vision loss in old age is not seen as a disability, it’s seen as something else.
Isolated yet more dependent on others
Global trends show a worrying conundrum. Older people with dual sensory impairment become more socially isolated, which impacts their mental health and wellbeing. At the same time they can become increasingly dependent on other people to help them navigate and manage day-to-day activities with limited sight and hearing.
One aspect of this is how effectively they can comprehend and communicate in a health-care setting. Recent research shows doctors and nurses in hospitals aren’t making themselves understood to most of their patients with dual sensory impairment. Good communication in the health context is about more than just “knowing what is going on”, researchers note. It facilitates:
- shorter hospital stays
- fewer re-admissions
- reduced emergency room visits
- better treatment adherence and medical follow up
- less unnecessary diagnostic testing
- improved health-care outcomes.
‘Too hard’
Globally, there is a better understanding of how important it is to maintain active social lives as people age. But this is difficult for older adults with dual sensory loss. One person told us
I don’t particularly want to mix with people. Too hard, because they can’t understand. I can no longer now walk into that room, see nothing, find my seat and not recognise [or hear] people.
Again, these experiences increase reliance on family. But caring in this context is tough and largely hidden. Family members describe being the “eyes and ears” for their loved one. It’s a 24/7 role which can bring frustration, social isolation and depression for carers too. One spouse told us:
He doesn’t talk anymore much, because he doesn’t know whether [people are] talking to him, unless they use his name, he’s unaware they’re speaking to him, so he might ignore people and so on. And in the end, I noticed people weren’t even bothering him to talk, so now I refuse to go. Because I don’t think it’s fair.
So, what can we do?
Dual sensory impairment is a growing problem with potentially devastating impacts.
It should be considered a unique and distinct disability in all relevant protections and policies. This includes the right to dedicated diagnosis and support, accessibility provisions and specialised skill development for health and social professionals and carers.
We need to develop resources to help people with dual sensory impairment and their families and carers understand the condition, what it means and how everyone can be supported. This could include communication adaptation, such as social haptics (communicating using touch) and specialised support for older adults to navigate health care.
Increasing awareness and understanding of dual sensory impairment will also help those impacted with everyday engagement with the world around them – rather than the isolation many feel now.
Moira Dunsmore, Senior Lecturer, Sydney Nursing School, Faculty of Medicine and Health, University of Sydney, University of Sydney; Annmaree Watharow, Lived Experience Research Fellow, Centre for Disability Research and Policy, University of Sydney, and Emily Kecman, Postdoctoral research fellow, Department of Linguistics, University of Sydney
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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The Longevity Diet – by Dr. Valter Longo
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Another book with “The New Science” in its subtitle, so, is this one a new science?
Yes and no; some findings are new, many are not, what really sets this book apart from many of its genre though is that rather than focusing on fighting aging, it focuses on retaining youth. While this may seem like one and the same thing, there is a substantive difference beyond the ideological, which is: while anti-aging research focuses on what causes people to suffer age-related decline and fights each of those things, Dr. Longo’s research focuses on what is predominant in youthful bodies, cells, DNA, and looks to have more of that. Looking in a slightly different place means finding slightly different things, and knowledge is power indeed.
Dr. Longo bases his research and focus on his “5 pillars of longevity”. We’ll not keep them a mystery; they are:
- Juventology research
- Epidemiology
- Clinical studies
- Centenarian studies
- Study of complex systems
The first there (juventology research) may sound like needless jargon, but it is the counterpoint of the field of gerontology, and is otherwise something that didn’t have an established name.
You may wonder why “clinical studies” gets a separate item when the others already include studies; this is because many studies when it comes to aging and related topics are population-based studies, cohort studies, observational studies, or (as is often the case) multiple of the above at once.
Of course, all this discussion of academia is not itself practical information for the reader (unless we happen to work in the field), but it is interesting and does give confidence in the conclusions upon which the practical parts of the book are based.
And what are they? As the title suggests, it’s about diet, and specifically, it’s about Dr. Longo’s “fast-mimicking diet”, which boasts the benefits of intermittent fasting without intermittent fasting. This hinges, of course, on avoiding metabolic overload, which can be achieved with a fairly simple diet governed by the principles outlined in this book, based on the research referenced.
In the category of subjective criticism, there is quite a bit of fluff, much of it self-indulgently autobiographical and very complimentary, but its presence does not take anything away from the excellent content contained in the book.
Bottom line: if you’d like a fresh perspective on regaining/retaining youthfulness, then this is a great book to read.
Click here to check out The Longevity Diet, and stay younger!
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When Bad Joints Stop You From Exercising (5 Things To Change)
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The first trick to exercising with bad joints is to have better joints.
Now, this doesn’t necessarily mean you can take a supplement and magically your joint problems will be cured, but there are adjustable lifestyle factors that can and will make things relatively better or worse.
We say “and will”, because you don’t get a choice in that part. Everything we do, every little choice in our day, makes our health a little better or a little worse in some aspect(s). But we do get a choice between “relatively better” and “relatively worse”.
With that in mind, do check out:
- Avoiding/Managing Osteoarthritis
- Avoiding/Managing Rheumatoid Arthritis
- How To Really Look After Your Joints
Ok, you have bad joints though; what next?
Let’s assume you’re doing your best with the above, and/or have simply decided not to, which is your call. You know your circumstances best. Either way, your joints are still not in sufficiently good condition to be able to exercise the way you’d like.
First, the obvious: enjoy low-impact exercises
For example:
- Swimming
- Yoga (much more appropriate here than the commonly-paired “and tai chi”)*
- Isometric exercises (i.e. exercise without movement, e.g. squeezing things, or stationary stability exercises)
*This is not to say that tai chi is bad. But if your problem is specifically your knees, there are many movements in most forms of tai chi that require putting the majority of one’s weight on one bent leg, which means the knee of that leg is going to suffer. If your knees are fine, then this won’t be an issue and it will simply continue strengthening your knees without discomfort. But they have to be fine first.
See also: Exercising With Osteoporosis
Second: support your joints through a full range of motion
If you have bad joints, you probably know that there’s an unfortunate paradox whereby you get to choose between:
- Exercise, and inflame your joints
- Rest, and your joints seize up
This is the way to get around that damaging dilemma.
Moving your joints through a full range of motion regularly is critical for their maintenance, so do that in a way that isn’t straining them:
If it’s your shoulders, for example, you can do (slow, gentle!) backstroke or front-crawl or butterfly motions while standing in the comfort of your living room.
If it’s your knees, then supported squats can do you a world of good. That means, squat in front of a table or other stable object, with your fingertips (or as much of your hands as you need) on it, to take a portion of your weight (it can be a large portion; that’s fine too!) while you go through the full range of motion of the squat. Repeat.
And so forth for other joints.
See also: The Most Underrated Hip Mobility Exercise (Not Stretching)
Third: work up slowly, and stop early
You can do exercises that involve impact, and if you live a fairly normal life, you’ll probably have to (walking is an impact exercise). You can also enjoy cycling (low-impact, but not so low-impact as we discussed in the last section) and work up to running if you want to.
However…
While building up your joints’ mobility and strength, it is generally a good idea to stop before you think you need to.
This means that it’s important to do those exercises in a way that you can stop early. For example, an exercise bike or a treadmill can be a lot of use here, so that you don’t find you need to stop for the day while miles from your house.
If you get such a device, it doesn’t even have to be fancy and/or expensive. This writer got herself an inexpensive exercise bike like this one, and it’s perfectly adequate.
Fourth: prioritize recovery, even if it doesn’t feel like you need it
Everyone should do this anyway, but if your joints are bad, it goes double:
Overdone It? How To Speed Up Recovery After Exercise (According To Actual Science)
Fifth: get professional help
Physiotherapists are great for this. Find one, and take their advice for your specific body and your specific circumstances and goals.
Take care!
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A Tale Of Two Cinnamons
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Cinnamon’s Health Benefits (But Watch Out!)
Cinnamon is enjoyed for its sweet and punchy flavor. It also has important health properties!
Let’s take a look at the science…
A Tale Of Two Cinnamons
In your local supermarket, there is likely “cinnamon” and if you’re lucky, also “sweet cinnamon”. The difference between these is critical to understand before we continue:
“Cinnamon” = Cinnamomum cassia or Cinnamomum aromaticum. This is cheapest and most readily available. It has a relatively high cinnamaldehyde content, and a high coumarin content.
“Sweet cinnamon” Cinnamomum verum or Cinnamomum zeylanicum. It has a lower cinnamaldehyde content, and/but a much lower (almost undetectable) coumarin content.
You may be wondering: what’s with the “or” in both of those cases? Each simply has two botanical names in use. It’s inconvenient and confusing, but that’s how it is.
Great! What’s cinnamaldehyde and what’s coumarin?
Cinnamaldehyde is what gives cinnamon its “spice” aspect; it’s strong and fragrant. It also gives cinnamon most of its health benefits.
As a quick aside: it’s also used as the flavoring element in cinnamon flavored vapes, and in that form, it can cause health problems. So do eat it, but we recommend not to vape it.
Coumarin is toxic in large quantities.
The recommended safe amount is 0.1mg/kg, so you could easily go over this with a couple of teaspoons of cassia cinnamon:
Toxicology and risk assessment of coumarin: focus on human data
…while in Sweet/True/Ceylon cinnamon, those levels are almost undetectable:
Medicinal properties of ‘true’ cinnamon (Cinnamomum zeylanicum): a systematic review
If you have a cinnamon sensitivity, it is likely, but not necessarily, tied to the coumarin content rather than the cinnamaldehyde content.
Summary of this section before moving on:
“Cinnamon”, or cassia cinnamon, has about 50% stronger health benefits than “Sweet Cinnamon”, also called Ceylon cinnamon.
“Cinnamon”, or cassia cinnamon, has about 250% stronger health risks than “Sweet Cinnamon”, also called Ceylon cinnamon.
The mathematics here is quite simple; sweet cinnamon is the preferred way to go.
The Health Benefits
We spent a lot of time/space today looking at the differences. We think this was not only worth it, but necessary. However, that leaves us with less time/space for discussing the actual benefits. We’ll summarize, with links to supporting science:
“Those three things that almost always go together”:
Heart and blood benefits:
- Reduces triglyceride levels
- Reduces high blood pressure
- Reduces insulin insensitivity
- Reduces fasting blood sugar levels
Neuroprotective benefits:
The science does need more testing in these latter two, though.
Where to get it?
You may be able to find sweet cinnamon in your local supermarket, or if you prefer capsule form, here’s an example product on Amazon
Enjoy!
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Black Beans vs Pinto Beans – Which is Healthier?
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Our Verdict
When comparing black beans to pinto beans, we picked the pinto beans.
Why?
Both of these beans have won all their previous comparisons, so it’s no surprise that this one was very close. Despite their different appearance, taste, and texture, their nutritional profiles are almost identical:
In terms of macros, pinto beans have a tiny bit more protein, carbs, and fiber. So, a nominal win for pinto beans, but again, the difference is very slight.
When it comes to vitamins, black beans have more of vitamins A, B1, B3, and B5, while pinto beans have more of vitamins B2, B6, B9, C, E, K and choline. Superficially, again this is nominally a win for pinto beans, but in most cases the differences are so slight as to be potentially the product of decimal place rounding.
In the category of minerals, black beans have more calcium, copper, iron, and phosphorus, while pinto beans have more magnesium, manganese, selenium, and zinc. That’s a 4:4 tie, but the only one with a meaningful margin of difference is selenium (of which pinto beans have 4x more), so we’re calling this one a very modest win for pinto beans.
All in all, adding these up makes for a “if we really are pressed to choose” win for pinto beans, but honestly, enjoy either in accordance with your preference (this writer prefers black beans!), or better yet, both.
Want to learn more?
You might like to read:
What’s Your Plant Diversity Score?
Take care!
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Taking A Trip Through The Evidence On Psychedelics
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In Tuesday’s newsletter, we asked you for your opinions on the medicinal use of psychedelics, and got the above-depicted, below-described, set of responses:
- 32% said “This is a good, evidence-based way to treat many brain disorders”
- 32% said “There are some benefits, but they don’t outweigh the risks”
- 20% said “This can help a select few people only; useless for the majority”
- 16% said “This is hippie hogwash and hearsay; wishful thinking at best”
Quite a spread of answers, so what does the science say?
This is hippie hogwash and hearsay; wishful thinking at best! True or False?
False! We’re tackling this one first, because it’s easiest to answer:
There are some moderately-well established [usually moderate] clinical benefits from some psychedelics for some people.
If that sounds like a very guarded statement, it is. Part of this is because “psychedelics” is an umbrella term; perhaps we should have conducted separate polls for psilocybin, MDMA, ayahuasca, LSD, ibogaine, etc, etc.
In fact: maybe we will do separate main features for some of these, as there is a lot to say about each of them separately.
Nevertheless, looking at the spread of research as it stands for psychedelics as a category, the answers are often similar across the board, even when the benefits/risks may differ from drug to drug.
To speak in broad terms, if we were to make a research summary for each drug it would look approximately like this in each case:
- there has been research into this, but not nearly enough, as “the war on drugs” may well have manifestly been lost (the winner of the war being: drugs; still around and more plentiful than ever), but it did really cramp science for a few decades.
- the studies are often small, heterogenous (often using moderately wealthy white student-age population samples), and with a low standard of evidence (i.e. the methodology often has some holes that leave room for reasonable doubt).
- the benefits recorded are often small and transient.
- in their favor, though, the risks are also generally recorded as being quite low, assuming proper safe administration*.
*Illustrative example:
Person A takes MDMA in a club, dances their cares away, has had only alcohol to drink, sweats buckets but they don’t care because they love everyone and they see how we’re all one really and it all makes sense to them and then they pass out from heat exhaustion and dehydration and suffer kidney damage (not to mention a head injury when falling) and are hospitalized and could die;
Person B takes MDMA in a lab, is overwhelmed with a sense of joy and the clarity of how their participation in the study is helping humanity; they want to hug the researcher and express their gratitude; the researcher reminds them to drink some water.
Which is not to say that a lab is the only safe manner of administration; there are many possible setups for supervised usage sites. But it does mean that the risks are often as much environmental as they are risks inherent to the drug itself.
Others are more inherent to the drug itself, such as adverse cardiac events for some drugs (ibogaine is one that definitely needs medical supervision, for example).
For those who’d like to see numbers and clinical examples of the bullet points we gave above, here you go; this is a great (and very readable) overview:
NIH | Evidence Brief: Psychedelic Medications for Mental Health and Substance Use Disorders
Notwithstanding the word “brief” (intended in the sense of: briefing), this is not especially brief and is rather an entire book (available for free, right there!), but we do recommend reading it if you have time.
This can help a select few people only; useless for the majority: True or False?
True, technically, insofar as the evidence points to these drugs being useful for such things as depression, anxiety, PTSD, addiction, etc, and estimates of people who struggle with mental health issues in general is often cited as being 1 in 4, or 1 in 5. Of course, many people may just have moderate anxiety, or a transient period of depression, etc; many, meanwhile, have it worth.
In short: there is a very large minority of people who suffer from mental health issues that, for each issue, there may be one or more psychedelic that could help.
This is a good, evidence-based way to treat many brain disorders: True or False?
True if and only if we’re willing to accept the so far weak evidence that we discussed above. False otherwise, while the jury remains out.
One thing in its favor though is that while the evidence is weak, it’s not contradictory, insofar as the large preponderance of evidence says such therapies probably do work (there aren’t many studies that returned negative results); the evidence is just weak.
When a thousand scientists say “we’re not completely sure, but this looks like it helps; we need to do more research”, then it’s good to believe them on all counts—the positivity and the uncertainty.
This is a very different picture than we saw when looking at, say, ear candling or homeopathy (things that the evidence says simply do not work).
We haven’t been linking individual studies so far, because that book we linked above has many, and the number of studies we’d have to list would be:
n = number of kinds of psychedelic drugs x number of conditions to be treated
e.g. how does psilocybin fare for depression, eating disorders, anxiety, addiction, PTSD, this, that, the other; now how does ayahuasca fare for each of those, and so on for each drug and condition; at least 25 or 30 as a baseline number, and we don’t have that room.
But here are a few samples to finish up:
- Psilocybin as a New Approach to Treat Depression and Anxiety in the Context of Life-Threatening Diseases—A Systematic Review and Meta-Analysis of Clinical Trials
- Therapeutic Use of LSD in Psychiatry: A Systematic Review of Randomized-Controlled Clinical Trials
- Efficacy of Psychoactive Drugs for the Treatment of Posttraumatic Stress Disorder: A Systematic Review of MDMA, Ketamine, LSD and Psilocybin
- Changes in self-rumination and self-compassion mediate the effect of psychedelic experiences on decreases in depression, anxiety, and stress.
- Psychedelic Treatments for Psychiatric Disorders: A Systematic Review and Thematic Synthesis of Patient Experiences in Qualitative Studies
- Repeated lysergic acid diethylamide (LSD) reverses stress-induced anxiety-like behavior, cortical synaptogenesis deficits and serotonergic neurotransmission decline
In closing…
The general scientific consensus is presently “many of those drugs may ameliorate many of those conditions, but we need a lot more research before we can say for sure”.
On a practical level, an important take-away from this is twofold:
- drugs, even those popularly considered recreational, aren’t ontologically evil, generally do have putative merits, and have been subject to a lot of dramatization/sensationalization, especially by the US government in its famous war on drugs.
- drugs, even those popularly considered beneficial and potentially lifechangingly good, are still capable of doing great harm if mismanaged, so if putting aside “don’t do drugs” as a propaganda of the past, then please do still hold onto “don’t do drugs alone”; trained professional supervision is a must for safety.
Take care!
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Can a drug like Ozempic help treat addictions to alcohol, opioids or other substances?
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Semaglutide (sold as Ozempic, Wegovy and Rybelsus) was initially developed to treat diabetes. It works by stimulating the production of insulin to keep blood sugar levels in check.
This type of drug is increasingly being prescribed for weight loss, despite the fact it was initially approved for another purpose. Recently, there has been growing interest in another possible use: to treat addiction.
Anecdotal reports from patients taking semaglutide for weight loss suggest it reduces their appetite and craving for food, but surprisingly, it also may reduce their desire to drink alcohol, smoke cigarettes or take other drugs.
But does the research evidence back this up?
Animal studies show positive results
Semaglutide works on glucagon-like peptide-1 receptors and is known as a “GLP-1 agonist”.
Animal studies in rodents and monkeys have been overwhelmingly positive. Studies suggest GLP-1 agonists can reduce drug consumption and the rewarding value of drugs, including alcohol, nicotine, cocaine and opioids.
Out team has reviewed the evidence and found more than 30 different pre-clinical studies have been conducted. The majority show positive results in reducing drug and alcohol consumption or cravings. More than half of these studies focus specifically on alcohol use.
However, translating research evidence from animal models to people living with addiction is challenging. Although these results are promising, it’s still too early to tell if it will be safe and effective in humans with alcohol use disorder, nicotine addiction or another drug dependence.
What about research in humans?
Research findings are mixed in human studies.
Only one large randomised controlled trial has been conducted so far on alcohol. This study of 127 people found no difference between exenatide (a GLP-1 agonist) and placebo (a sham treatment) in reducing alcohol use or heavy drinking over 26 weeks.
In fact, everyone in the study reduced their drinking, both people on active medication and in the placebo group.
However, the authors conducted further analyses to examine changes in drinking in relation to weight. They found there was a reduction in drinking for people who had both alcohol use problems and obesity.
For people who started at a normal weight (BMI less than 30), despite initial reductions in drinking, they observed a rebound increase in levels of heavy drinking after four weeks of medication, with an overall increase in heavy drinking days relative to those who took the placebo.
There were no differences between groups for other measures of drinking, such as cravings.
Some studies show a rebound increase in levels of heavy drinking. Deman/Shutterstock In another 12-week trial, researchers found the GLP-1 agonist dulaglutide did not help to reduce smoking.
However, people receiving GLP-1 agonist dulaglutide drank 29% less alcohol than those on the placebo. Over 90% of people in this study also had obesity.
Smaller studies have looked at GLP-1 agonists short-term for cocaine and opioids, with mixed results.
There are currently many other clinical studies of GLP-1 agonists and alcohol and other addictive disorders underway.
While we await findings from bigger studies, it’s difficult to interpret the conflicting results. These differences in treatment response may come from individual differences that affect addiction, including physical and mental health problems.
Larger studies in broader populations of people will tell us more about whether GLP-1 agonists will work for addiction, and if so, for whom.
How might these drugs work for addiction?
The exact way GLP-1 agonists act are not yet well understood, however in addition to reducing consumption (of food or drugs), they also may reduce cravings.
Animal studies show GLP-1 agonists reduce craving for cocaine and opioids.
This may involve a key are of the brain reward circuit, the ventral striatum, with experimenters showing if they directly administer GLP-1 agonists into this region, rats show reduced “craving” for oxycodone or cocaine, possibly through reducing drug-induced dopamine release.
Using human brain imaging, experimenters can elicit craving by showing images (cues) associated with alcohol. The GLP-1 agonist exenatide reduced brain activity in response to an alcohol cue. Researchers saw reduced brain activity in the ventral striatum and septal areas of the brain, which connect to regions that regulate emotion, like the amygdala.
In studies in humans, it remains unclear whether GLP-1 agonists act directly to reduce cravings for alcohol or other drugs. This needs to be directly assessed in future research, alongside any reductions in use.
Are these drugs safe to use for addiction?
Overall, GLP-1 agonists have been shown to be relatively safe in healthy adults, and in people with diabetes or obesity. However side effects do include nausea, digestive troubles and headaches.
And while some people are OK with losing weight as a side effect, others aren’t. If someone is already underweight, for example, this drug might not be suitable for them.
In addition, very few studies have been conducted in people with addictive disorders. Yet some side effects may be more of an issue in people with addiction. Recent research, for instance, points to a rare risk of pancreatitis associated with GLP-1 agonists, and people with alcohol use problems already have a higher risk of this disorder.
Other drugs treatments are currently available
Although emerging research on GLP-1 agonists for addiction is an exciting development, much more research needs to be done to know the risks and benefits of these GLP-1 agonists for people living with addiction.
In the meantime, existing effective medications for addiction remain under-prescribed. Only about 3% of Australians with alcohol dependence, for example, are prescribed medication treatments such as like naltrexone, acamprosate or disulfiram. We need to ensure current medication treatments are accessible and health providers know how to prescribe them.
Continued innovation in addiction treatment is also essential. Our team is leading research towards other individualised and effective medications for alcohol dependence, while others are investigating treatments for nicotine addiction and other drug dependence.
Read the other articles in The Conversation’s Ozempic series here.
Shalini Arunogiri, Addiction Psychiatrist, Associate Professor, Monash University; Leigh Walker, , Florey Institute of Neuroscience and Mental Health, and Roberta Anversa, , The University of Melbourne
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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